LOWER GI PATHOLOGY
Inflammatory conditions
active
neutrophil infiltration (characteristic), cryptitis, normal architecture
chronic
crypt architectural distortion (branching/shortening)
active chronic inflammation - acute + evidence of chronicity
crypt abscesses (neutrophil infiltration into lumen of crypts)
Infective colitis
Ischaemic colitis
Diverticulitis
Idiopathic IBD
acute colitis
acute colitis
active or active chronic colitis
active chronic colitis
pseudomembranous colitis
due to C. difficile infection following broad spectrum antibiotics
neutrophils form 'membrane' on top of mucosa
acute inflammation, neutrophils, mild crypt loss
watery diarrhoea, colicky abdominal pain, fever
usually superficial
if penetrates through the colon wall, causes infarction
mixed acute and chronic inflammation, crypt loss
lack of O2 supply (usually due to decreased blood flow)
causes: arterial/venous occlusion, vasculitis, intestinal obstruction
most commonly occurs in the watershed area around splenic flexure/descending colon
between supply of middle and left colic arteries
outpouching of mucosal wall (where muscle is weakest)
bacteria can overgrow here
if obstructed, they perforate or form diverticular abscess
bleeding, perforation, abscess, fistula (if adherent to other structures), stricture
Ulcerative colitis
acute
marked hyperaemia and irregular ulceration
chronic
diffuse ulceration with focal residual mucosa
pseudopolyps (formed by regenerating mucosa)
total mucosal atrophy and crypt flattening (late)
diffuse active inflammation confined to mucosa
basal plasmacytosis, crypt distortion
complications
toxic megacolon (perforation)
dysplasia and carcinoma (>20 years)
Crohn's disease
involves any site in GIT (most commonly terminal ileum)
patchy (skip lesions)
affects full thickness of bowel wall
fat wrapping
thick rigid wall
longitudinal ulceration with sharp demarcation
cobblestone appearance (due to regenerating mucosa between ulcerations)
deep fissures
muscle and neural hypertrophy
granulomas in 50%
collection of epithelioid histiocytes (macrophages)
complications
adhesions, perforations, abscess, fistula, stricture, dysplasia/carcinoma
Neoplastic disease
primary
secondary
metastasis
epithelial (most common)
Lymphoid
soft tissue
glandular epithelium
adenoma (polyp)
carcinoma
neuroendocrine cells
neuroendocrine tumour
sessile (flat on surface)
pedunculated (long stalk of mucosa)
neoplastic
non-neoplastic
adenomatous polyp
serrated polyp
reactive (inflammatory or traumatic)
hyperplastic
hamartomatous (developmental)
Peutz-Jegher's polyp
juvenile polyp
tubular adenoma
villous adenoma
tubulovillous adenoma
typically sessile
typically pedunculated
traditional serrated
sessile serrated
most polyps are sporadic not genetic
familial polyposis syndromes
familial adenomatous polyposis (FAP)
100+ polyps
develop carcinoma <40 years (100%)
total colectomy
abnormal glandular tissue
chromosome instability pathway
oncogenes (e.g. ß-catenin) and tumour suppressor genes (e.g. APC, e-cadherin)
tend to be left-sided carcinomas
microsatellite instability pathway
DNA mismatch repair due to gene mutation or promoter methylation (silencing)
tend to be right-sided carcinomas
better prognosis
autosomal dominant mutation of APC gene (Ch5)
attenuated FAP
MYH or APC gene (other loci)
less than 100 polyps
lynch (HNPCC)
less than 100 polyps
DNA mismatch repair genes MSH2/MLH1/MSH6/PMS2
risk of developing carcinoma >50 years
risk of developing carcinoma 45-50 years